Overview

Brief Summary

Streptococcus

Streptococcus is a genus of spherical Gram-positive bacteria belonging to the phylum Firmicutes and the lactic acid bacteria group. Cellular division occurs along a single axis in these bacteria, and thus they grow in chains or pairs, hence the name — from Greek στρεπτος streptos, meaning easily bent or twisted, like a chain (twisted chain). Contrast this with staphylococci, which divide along multiple axes and generate grape-like clusters of cells. Most streptococci are oxidase- and catalase-negative, and many are facultative anaerobes.

Species of Streptococcus are classified based on their hemolytic properties.[5] Alpha-hemolytic species cause oxidization of iron in hemoglobin molecules within red blood cells, giving it a greenish color on blood agar. Beta-hemolytic species cause complete rupture of red blood cells. On blood agar, this appears as wide areas clear of blood cells surrounding bacterial colonies. Gamma-hemolytic species cause no hemolysis.

Beta-hemolytic streptococci are further characterised by Lancefieldserotyping, which describes specific carbohydrates present on the bacterial cell wall.[6] The 20 described serotypes are named Lancefield groups A to V (excluding I and J).

In the medical setting, the most important groups are the alpha-hemolytic streptococci S. pneumoniae and Streptococcusviridans group, and the beta-hemolytic streptococci of Lancefield groups A and B (also known as “group A strep” and “group B strep”).

S. pneumoniae (sometimes called pneumococcus), is a leading cause of bacterial pneumonia and occasional etiology of otitis media, sinusitis, meningitis, and peritonitis. Inflammation is thought to be the major cause of how pneumococci cause disease, hence the tendency of diagnoses associated with them to involve inflammation.

Additional complications may be caused by GAS, namely acute rheumatic fever and acute glomerulonephritis. Rheumatic fever, a disease that affects the joints, kidneys, and heart valves, is a consequence of untreated strep A infection caused not by the bacterium itself. Rheumatic fever is caused by the antibodies created by the immune system to fight off the infection cross-reacting with other proteins in the body. This "cross-reaction" causes the body to essentially attack itself and leads to the damage above. Globally, GAS has been estimated to cause more than 500,000 deaths every year, making it one of the world's leading pathogens.[7] Group A Streptococcus infection is generally diagnosed with a rapid strep test or by culture.

S. agalactiae, or group B Streptococcus, GBS, causes pneumonia and meningitis in neonates and the elderly, with occasional systemic bacteremia. They can also colonize the intestines and the female reproductive tract, increasing the risk for premature rupture of membranes during pregnancy, and transmission of the organism to the infant. The American College of Obstetricians and Gynecologists, American Academy of Pediatrics, and the Centers for Disease Control recommend all pregnant women between 35 and 37 weeks gestation to be tested for GBS. Women who test positive should be given prophylactic antibiotics during labor, which will usually prevent transmission to the infant.[9]

The United Kingdom has chosen to adopt a risk factor-based protocol, rather than the culture-based protocol followed in the US. Current guidelines state that if one or more of the following risk factors are present, then women should be treated with intrapartum antibiotics:

Preterm labour (<37 weeks)

Prolonged rupture of membranes (>18 hours)

Intrapartum fever (>38C)

Prior GBS affected infant

GBS bacteriuria during this pregnancy

This protocol results in treatment of 15–20% of pregnant women and prevention of 65–70% of cases of early onset GBS sepsis. [10]

This group includes S. equi, which causes strangles in horses,[11] and S. zooepidemicus—S. equi is a clonal descendent or biovar of the ancestral S. zooepidemicus—which causes infections in several species of mammals, including cattle and horses. S. dysgalactiae is also a member of group C, β-haemolytic streptococci that can cause pharyngitis and other pyogenic infections similar to group A streptococci.

Many former group D streptococci have been reclassified and placed in the genus Enterococcus (including E. faecalis, E. faecium, E. durans, and E. avium).[12] For example, Streptococcus faecalis is now Enterococcus faecalis.

Nonhemolytic streptococci rarely cause illness. However, weakly hemolytic group D beta-hemolytic streptococci and Listeria monocytogenes (which is actually a Gram-positive bacillus) should not be confused with nonhemolytic streptococci.

Group F streptococci were first described in 1934 by Long and Bliss amongst the "minute haemolytic streptococci".[13] They are also known as Streptococcus anginosus (according to the Lancefield classification system) or as members of the S. milleri group (according to the European system).

Group H streptococci cause infections in medium-sized canines. Group H streptococci rarely cause illness unless a human has direct contact with the mouth of a canine. One of the most common ways this can be spread is human-to-canine, mouth-to-mouth contact. However, the canine may lick the human's hand and infection can be spread, as well.[14]

Phylogenetic tree of Streptococcus species, based on data from PATRIC.[15] 16S groups are indicated by brackets and their key members are highlighted in red.

Streptococci have been divided into six groups on the basis of their 16S rDNA sequences: S. anginosus, S.bovis, S. mitis, S. mutans, S. pyogenes and S. salivarius.[16] The 16S groups have been confirmed by whole genome sequencing (see figure). The important pathogens S. pneumoniae and S. pyogenes belong to the S. mitis and S. pyogenes groups, respectively, while the causative agent of dental caries, Streptococcus mutans, is basal to the Streptococcus group.

The genomes of hundreds of species have been sequenced.[18] Most Streptococcus genomes are 1.8 to 2.3 Mb in size and encode 1,700 to 2,300 proteins. Some important genomes are listed in the table.[19] The four species shown in the table (S. pyogenes, S. agalactiae, S. pneumoniae, and S. mutans) have an average pairwise protein sequence identity of about 70%.[19]

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Viridans streptococci

The viridans streptococci are a large group of commensalstreptococcal bacteria species that are either α-hemolytic, producing a green coloration on blood agar plates (hence the name "viridans", from Latin "vĭrĭdis", green), or nonhemolytic. The pseudotaxonomic non-Linnean term Streptococcus viridans is often used to refer to this group of species, but writers that do not like to use the pseudotaxonomic term (which treats a group of species as if they were one species) prefer the terms viridans streptococci[1] or viridans streptococcal species.

The organisms are most abundant in the mouth, and one member of the group, S. mutans, is the etiologic agent of dental caries in most cases and populations. S. sanguinis is also another potential cause. Others may be involved in other mouth or gingival infections as pericoronitis.

Viridans streptococci have the unique ability to synthesize dextrans from glucose, which allows them to adhere to fibrin-platelet aggregates at damaged heart valves. This mechanism underlies their ability to cause subacute valvular heart disease following their introduction into the bloodstream (e.g., following dental extraction).

Streptococcus milleri group

Streptococcus milleri is an unofficial name applied to a group of basically similar viridans streptococci species[1] showing various hemolytic, serological, and physiological characteristics. The species name Streptococcus anginosus has recently been recognized as the approved name for these organisms. They have been implicated as etiologic agents in a variety of serious purulent infections, but because of their heterogeneous characteristics, these organisms may be unrecognized or misidentified by clinical laboratorians.[2] The unique characteristic of them from other pathogenic streptococci, such as S. pyogenes and S. agalactiae, is their ability to cause abscesses.[3][4]

These non-hemolytic viridans streptococci were first described by Guthof in 1956 after being isolated from dental abscesses. He named these organisms "Streptococcus milleri" in honor of the microbiologist W. D. Miller.[5][6] Ehy UOu Pnis